Anticoagulants Plus Streptokinase Therapy in Progressive Stroke

Meyer, John Stirling; Gilroy, John; Barnhart, Marion I.; Johnson, Jared

doi:10.1001/jama.1964.03070050039011

Cited by 75 publications

(21 citation statements)

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“…Patients treated with SK demonstrated significantly higher mortality and a higher incidence of cerebral hemorrhage at autopsy. 4 Patients treated with plasmin had no hemorrhagic complications and showed no difference in clinical outcome compared with untreated patients. 5 In both of these studies, however, thrombolytic therapy was followed by treatment with heparin, which itself is known to produce cerebral hemorrhage in stroke.…”

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confidence: 89%

Hemorrhagic complications of thrombolytic therapy in experimental stroke.

Slivka

Pulsinelli

1987

Stroke

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Recent success with thrombolytic therapy for acute myocardial infarction has stimulated interest in its use for stroke. To determine the hemorrhagic potential of thrombolytic therapy in experimental cerebral infarction, we compared a group of tissue plasminogen activator-treated rabbits (a = 4) with 2 groups of streptokinase-treated rabbits (n = 6 in each), as well as with 3 groups of heparin-treated rabbits (n = 5 in each) and untreated controls (n = 12). Focal cerebral infarction was produced in rabbits by occlusion of the right common carotid and middle cerebral arteries coupled with 2 hours of halothane-induced hypotension. Treatment with heparin or thrombolytic agents began 24 hours after occlusion. One additional group was treated with streptokinase 1 hour after occlusion (n = 6) to determine the hemorrhagic potential of thrombolytic agents in evolving infarction. Rabbits were killed 29-33 hours after occlusion, and brain sections were examined using light microscopy. The results demonstrate that microscopic hemorrhage is frequently present in infarcted tissue irrespective of treatment. Gross cerebral hemorrhage did not occur in untreated rabbits or in rabbits treated with streptokinase 1 hour after occlusion. Only rabbits treated with streptokinase, tissue plasminogen activator, or excessive doses of heparin 24 hours after occlusion, at a time when cerebral infarction was well established, exhibited gross hemorrhage in the area of infarction. These data suggest that treatment of ischemic stroke with thrombolytic agents carries an increased risk of cerebral hemorrhage unless the agents are given early after the onset of symptoms. (Stroke 1987;18:1148-1156)

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confidence: 89%

Hemorrhagic complications of thrombolytic therapy in experimental stroke.

Slivka

Pulsinelli

1987

Stroke

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“…Of the six randomized trials shown in Table 1 and Figure 1, the two by Meyer et al 12 - 13 were conducted before the invention of computed tomographic (CT) scanning, and therefore some patients with primary intracerebral hemorrhage or hemorrhagic infarction may inadvertently have been included. The numbers were small, and the outcome measure was clinical evaluation at 10 days, which may be too early for valid assessment.…”

Section: Randomized Trialsmentioning

confidence: 99%

Thrombolysis in acute ischemic stroke: does it work?

Wardlaw

Warlow

1992

Stroke

164

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Background: This article is presented to provoke further discussion regarding the use of thrombolj drugs to treat acute ischemic stroke.Summary of Review: Overview analysis of the six randomized trials of thrombolysis in acute ischer stroke available in the world literature shows a 20% increase in the odds of death and a 30% reduction the odds of death or deterioration (both with wide confidence intervals, neither result significant) af thrombolytic treatment for acute ischemic stroke. Exclusion of the two trials conducted without I benefit of computed tomographic scanning shows a 37% reduction in the odds of death (95% confidence interval, 74% reduction to 40% excess) and a significant reduction of 56% in the odds of death or deterioration after thrombolytic treatment (95% confidence interval, 20-76% reduction; 2p=0.007). Analysis of all published studies (randomized and nonrandomized) shows that there does not appear to be an excess risk of hemorrhagic transformation of the cerebral infarct or of severe edema formation.Conclusions: We believe the present evidence is sufficiently encouraging to warrant proper testing of thrombolysis in sufficiently large and well-designed randomized clinical trials to influence clinical practice. (Stroke 1992;23:1826-1839 KEY WORDS • cerebral ischemia • clinical trials • thrombolytic therapy

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“…63 When the same group evaluated whether streptokinase and heparin could be given in progressive strokes within 72 hours of onset, they found that there was significantly worse outcomes with increased risk of ICH. 64 About 30 years later, streptokinase was used in multiple studies for myocardial infarction and was again looked at in the context of acute ischemic stroke; however, none of the trials, including the Multicenter Acute Stroke Trial-Europe (MAST-E), Multicenter Acute Stroke Trial-Italy (MAST-I), and the Australian Streptokinase study, were able to demonstrate a benefit for streptokinase administration versus placebo. 65,66 MAST-E demonstrated increased parenchymal bleeding, without an increase in overall symptomatic hemorrhage.…”

Section: Acute Stroke Treatments: Outcome Assessment In Thrombolysis mentioning

confidence: 99%

Evolving Treatments for Acute Ischemic Stroke

Zerna

Hegedus

Hill

2016

Circulation Research

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Abstract:The purpose of this article is to review advances in stroke treatment in the hyperacute period. With recent evolutions of technology in the fields of imaging, thrombectomy devices, and emergency room workflow management, as well as improvement in statistical methods and study design, there have been ground breaking changes in the treatment of acute ischemic stroke. We describe how stroke presents as a clinical syndrome and how imaging as the most important biomarker will help differentiate between stroke subtypes and treatment eligibility. The evolution of hyperacute treatment has led to the current standard of care: intravenous thrombolysis with tissue-type plasminogen activator and endovascular treatment for proximal vessel occlusion in the anterior cerebral circulation. All patients with acute ischemic stroke are in need of hyperacute secondary prevention because the risk of recurrence is highest closest to the index event. The dominant themes of modern stroke care are the use of neurovascular imaging and speed of diagnosis and treatment. (Circ Res.

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Anticoagulants Plus Streptokinase Therapy in Progressive Stroke

Cited by 75 publications

References 2 publications

Hemorrhagic complications of thrombolytic therapy in experimental stroke.

Hemorrhagic complications of thrombolytic therapy in experimental stroke.

Thrombolysis in acute ischemic stroke: does it work?

Evolving Treatments for Acute Ischemic Stroke

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